The spinal cord is the major conduit through which sensory and motor signals pass between brain and body. Damage to the spinal cord often results in devastating and persistent functional deficits. In general, adult CNS neurons can survive axotomy and react with an upregulation of proteins related to axonal growth (e.g. GAP-43). Lesioned axons can sprout spontaneously, but this regeneration attempt is transitory and no significant regrowth over long distances occurs. We are interested in understanding the cellular and molecular mechanisms that account for such abortive sprouting behaviors of regenerating axons. In addition to myelin associated inhibitors, recent studies have suggested a potential involvement of axonal repellents, such as semaphorins, in restricting axon regeneration after injury. Thus, in this study, we propose to perform a systematic study to examine if there is a correlation between semaphorin expression and axonal behaviors in spinal cord injury models. We will first characterize the terminal sprouting of lesioned axons and collateral sprouting of intact axons in two different but complementary spinal cord injury models. These axonal morphological responses will be related to the spatial and timing expression patterns of members of semaphorins and their receptor molecules in injured rat spinal cords. It is hoped that these studies will provide important insights into the potential involvement of sernaphorins in governing the postinjury axonal responses, which might be instructive for designing therapeutic strategies for spinal cord injury.